Evaluation of Immunohistochemical Expression of Heparanase in Helicobacter Pylori-Associated Chronic Gastritis

Chronic Gastritis Clinical Trial

Official title:

Evaluation of Immunohistochemical Expression of Heparanase in Helicobacter Pylori-Associated Chronic Gastritis

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT05073614
• Other study ID #: Soh-Med-21-09-43
• Status: Completed
• Phase: N/A
• Start date: July 1, 2021
• Est. completion date: January 1, 2022

Study information

• Verified date: January 2022
• Source: Sohag University
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

Treatment of H.pylori may not be achieved in many patients with chronic gastritis. Termination of the inflammatory respose produced by h.pylori may be useful in management of difficult cases. Heparanase is a pro-inflammatory mediator. Blocking of heparanase may relief the symptoms of chronic gastritis.

Description:

Chronic gastritis (CG) is a very common disease. The incidence of CG is not accurately known. However, it is clear that the incidence of CG is increasing by advancing age. CG is divided into two main types; type A or immune and type B or non-immune gastritis. Both types of CG share the same histological features. However, type A is less common, usually affects the gastric fundus in a diffuse manner and separates the antrum. on the contrary; type B or non-immune CG, which is by far more common, inevitably develops in the antrum and progresses proximally. H. pylori-induced CG usually requires antibiotic therapy to eradicate the causative organism and subsequently terminate the inflammatory response and the symptoms of gastritis. However, eradication of H. pylori is difficult to be achieved in many patients. Previous studies established that there is a vicious circle between H. pylori-infected gastric epithelial cells and the gastric mucosal inflammatory cells. Heparanase (HPSE) is a mammalian ᵦ-endoglucoronidase. HPSE plays a critical role in multiple inflammatory processes by degrading and remodeling heparan sulfate polysaccharide chains in the extracellular matrix (ECM). This leads to release of multiple cytokines and chemokines which are located in the ECM. HPSE is a drug target, three inhibitors of this enzyme have been tested in early stage clinical trials. Many studies reported that the expression of HPSE is up-regulated in a variety of inflammatory conditions as ulcerative colitis, acute pancreatitis, acute vasculitis and sepsis. The aim of this work is to evaluate the role of heparanase (HPSE) in chronic gastritis (CG) by correlating the expression of HPSE to different histological features of CG as presence of H. pylori, chronic inflammatory infiltrate, gastric atrophy, intestinal metaplasia and neutrophil infiltrate (activity), to detect new treatment modalities in CG.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 70
• Est. completion date: January 1, 2022
• Est. primary completion date: December 30, 2021
• Accepts healthy volunteers: No
• Gender: All
• Age group: N/A and older

Eligibility

Inclusion Criteria:

• patients with symptomatic chronic gastritis who underwent upper endoscopy.

Exclusion Criteria:

• patients with gastric carcinoma.

Related Conditions & MeSH terms

• Chronic Gastritis
• Gastritis
• Gastritis, Atrophic

Intervention

Genetic:
• immunohistochemical detection of Heparanase in chronic gastritis
immunohistochemical detection of Heparanase in chronic gastritis specimens.

Locations

Country	Name	City	State
Egypt	Maisa Hashem Mohammed	Sohag

Sponsors (1)

Lead Sponsor	Collaborator
Sohag University

Country where clinical trial is conducted

Egypt, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Correlation of Heparanase expression in chronic gastritis.	we will correlate the intensity and percentage of immunohistochemical expression of Heparanase to different parameters of chronic gastritis as severity of gastric atrophy, chronic inflammation, intensity of neutrophilic infiltrate and presence or absence of H. pylori.	6 months